An Unusual Cause of Syncope With T-Wave Abnormalities

Article Type
Article
Changed
Wed, 12/12/2018 - 20:50
Display Headline
An Unusual Cause of Syncope With T-Wave Abnormalities
A 34-year-old man presented for evaluation of syncope. He had a headache and had been vomiting over the past week.
Author(s)
Michael J. Bono, MD
Francis L. Counselman, MD

Case

A 34-year-old man presented to our ED via emergency medical services (EMS) following a syncopal episode. The patient stated that as he was getting ready for work earlier that morning, he experienced sudden lightheadedness and passed out, whereupon his wife immediately called EMS. The patient denied any previous history of syncope, but said he had been experiencing frequent episodes of nausea and vomiting over the past week. He also complained of a mild occipital headache that acetaminophen had failed to relieve.

The patient had been seen at a different ED 3 days earlier for nausea and vomiting. After evaluating the patient, the emergency physician (EP) at this facility felt the most likely cause of the patient’s gastrointestinal issues was related to hydralazine, his antihypertensive medication, and advised the patient to discontinue its use.

During evaluation at our ED, the patient denied fever, chills, neck stiffness, numbness, weakness, tingling of the extremities, or difficulty walking. He also denied chest pain, shortness of breath, or urinary symptoms. The patient’s medical history was significant only for hypertension; he had not taken any antihypertensive or other medications for the past 3 days, as previously instructed by the EP at the other ED. The patient denied alcohol or drug abuse.

On physical examination, the patient’s vital signs were: temperature, 98.6°F; heart rate, 58 beats/minute; blood pressure, 130/90 mm Hg; and respiratory rate, 16 breaths/minute. Oxygen saturation was 100% on room air. Examination of the head was normal and without evidence of trauma. Both pupils measured 4 mm and were equally round and reactive to light; the patient’s extraocular movements were intact. The remainder of the head, eyes, ears, nose, and throat examination was normal. The neck was supple, without masses or meningeal signs. The cardiopulmonary and abdominal examinations were all normal. On neurological examination, the patient was awake, alert, and oriented to person, place, and time. Cranial nerves II through XII were intact, and the patient had 5/5 motor strength in all four extremities and a normal gait.

 

 

 

Because we were concerned about the patient’s unexplained syncopal episode, we ordered laboratory tests, including a complete blood count (CBC), evaluation of electrolytes and glucose levels, and kidney function. In addition, we also ordered an electrocardiogram (ECG) and a noncontrast computed tomography (CT) scan of the head. All laboratory test results were within normal range. The ECG, however, demonstrated sinus bradycardia (approximately 58 beats/minute), a normal PR and QRS interval, a normal axis, and an incomplete right bundle branch block with tall, large, splayed upright T waves in the precordial leads (Figure). Based on the abnormal ECG results, we ordered serum cardiac marker studies, the values of which were all within normal range. The noncontrast CT scan of the head revealed a low-density posterior fossa mass compressing the fourth ventricle with secondary hydrocephalus.

The patient was placed with his head in an upright position and given 1 g/kg mannitol and 10 mg dexamethasone intravenously (IV). Neurosurgery services were consulted, and the patient underwent surgery the following morning. Surgery confirmed the presence of a hemangioblastoma. The hemangioblastoma was successfully excised, and the patient had an uneventful recovery. Interestingly, the significant T-wave changes in the precordial leads were no longer present postoperatively.

Discussion

Syncope and near-syncope are common reasons for ED visits. Syncope is a syndrome characterized by a transient, self-limited episode of loss of consciousness occurring as a result of a brief interruption of the oxygen supply to the brain.1 This interruption is almost always due to a transient cessation of blood flow.1 In true syncope (as opposed to seizures or hypoglycemia), the episode is characterized by a rapid onset of loss of consciousness—with or without warning symptoms.1 It is important to determine the cause of syncope, because 7% to 23% of such patients will suffer serious outcomes within 7 to 30 days of their ED visit—either within a hospital setting or at home.2

Etiology

There are many causes of syncope. In most cases, the etiology falls under one of three broad categories: neurally mediated (or reflex mediated), orthostatic hypotensive-mediated, or cardiovascular (CV)-mediated. Less common causes of syncope include cerebrovascular injury.1 The Table outlines both common and uncommon causes of syncope.

 

 

 

On presentation, our patient had several possible causes for his syncopal episode: an abnormal ECG (CV); multiple episodes of emesis (volume depletion); and headache (cerebrovascular). The EP worked up all three of these signs and symptoms simultaneously as is the appropriate protocol when evaluating an ED patient presenting with undifferentiated syncope.

Signs and Symptoms

Patients with undiagnosed brain tumors normally present with headache, seizures, nausea, vomiting, focal neurological deficits, or an altered mental status.3 Syncope is a very rare manifestation of a brain tumor3; however, our patient did complain of headache, nausea, and vomiting.

In addition to the unusual cause of the syncope, the abnormally large upright T waves make this case even more notable. T-wave changes are the most common ECG abnormality, seen in about 50% of abnormal tracings reviewed in a hospital population and in 2.4% of all ECGs.4

In general, T-wave changes are a result of local changes in the duration of repolarization. T-wave inversion is the most common T-wave abnormality and is typically observed in the setting of ischemia, post-ingestion of food, following an episode of tachycardia or anxiety, and autonomic dysfunction.5 However, in patients who have a cerebral etiology (usually hemorrhage), the T-wave changes may be either upright (as in our case) or inverted.5 Historically, subarachnoid hemorrhage (SAH) has been associated with ST-segment elevation and T-wave inversion. Hypothalamic stimulation and autonomic dysfunction have been linked to abnormal T-waves, but this has not been conclusively proven to be the cause of the abnormality.6 For all of the aforementioned reasons, the specificity for a given cause of T-wave changes is exceedingly low.5

Hyperacute T-wave amplitude, with prominent symmetrical T waves in at least two continuous leads, may be the earliest sign of acute transmural myocardial infarction (MI).7 It usually persists for only a brief time before other ECG findings of acute MI are observed. Other common causes of hyperacute T waves include hyperkalemia (usually narrow-based, and peaked), early repolarization, left ventricular hypertrophy, and acute myocarditis.8 Less common causes of prominent T waves include pre-excitation  syndromes, pericarditis, and scorpion stings.9,10

Summary

It is unclear why our patient, who had a hemangioblastoma, demonstrated hyperacute T-wave abnormality on ECG. The abnormal upright T waves may have occurred secondary to the same theories regarding SAH, hypothalamic stimulation, or autonomic dysfunction. Regardless of the underlying etiology, this case serves as a reminder to the EP that not all T-wave changes on ECG are cardiac in origin. 

References

1.    Puppala VK, Dickinson O, Benditt DG. Syncope: classification and risk stratification. J Cardiol. 2014;63(3):171-177.

2.    Thiruganasambandamoorthy V, Stiell IG, Sivilotti ML, et al. Risk stratification of adult emergency department syncope patients to predict short-term serious outcomes after discharge (RiSEDS) study. BMC Emerg Med. 2014;14(1):8.

3.    van der Sluijs BM, Renier WO, Kappelle AC. Brain tumor as a rare cause of cardiac syncope. J Neurooncol. 2004;67(1-2):241-244.

4.    Friedberg CK, Zagar A. Nonspecific ST and T-wave changes. Circulation. 1961;23:665-661.

5.    Fisch C. T wave abnormalities due to extracardiac “functional” causes. ACC Curr J Rev. 1997;6(2):101-104.

6.    Chatterjee S. ECG changes in subarachnoid hemorrhage: a synopsis. Neth Heart J. 2011;19(1):31-47.

7.    Vojáčeka, J, Janskýb P, Janotac T. Third universal definition of myocardial infarction. Cor Vasa. 2013;55:e228-e235.

8.    Levis JT. ECG diagnosis: hyperacute T waves. Perm J. 2015;19(3):79.

9.    Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002;20(3):243-251.

10.   Kumar MR, Bharath RV, Subrahmanyam BV, Rammohan P, Agrawal A. Scorpion envenomation and its management in adults. Sahel Med J. 2013;16(2):60-63.

Article PDF
em048080364.pdf
Author and Disclosure Information

Michael J. Bono, MD; Francis L. Counselman, MD

Issue
Emergency Medicine - 48(8)
Publications
Emergency Medicine
MDedge Emergency Medicine
Page Number
364-366
Legacy Keywords
case report, syncope, t-wave, abnormalities, headache, case
Sections
Case Reports
Author(s)
Michael J. Bono, MD
Francis L. Counselman, MD
Author(s)
Michael J. Bono, MD
Francis L. Counselman, MD
Author and Disclosure Information

Michael J. Bono, MD; Francis L. Counselman, MD

Author and Disclosure Information

Michael J. Bono, MD; Francis L. Counselman, MD

Article PDF
em048080364.pdf
Article PDF
em048080364.pdf
A 34-year-old man presented for evaluation of syncope. He had a headache and had been vomiting over the past week.
A 34-year-old man presented for evaluation of syncope. He had a headache and had been vomiting over the past week.

Case

A 34-year-old man presented to our ED via emergency medical services (EMS) following a syncopal episode. The patient stated that as he was getting ready for work earlier that morning, he experienced sudden lightheadedness and passed out, whereupon his wife immediately called EMS. The patient denied any previous history of syncope, but said he had been experiencing frequent episodes of nausea and vomiting over the past week. He also complained of a mild occipital headache that acetaminophen had failed to relieve.

The patient had been seen at a different ED 3 days earlier for nausea and vomiting. After evaluating the patient, the emergency physician (EP) at this facility felt the most likely cause of the patient’s gastrointestinal issues was related to hydralazine, his antihypertensive medication, and advised the patient to discontinue its use.

During evaluation at our ED, the patient denied fever, chills, neck stiffness, numbness, weakness, tingling of the extremities, or difficulty walking. He also denied chest pain, shortness of breath, or urinary symptoms. The patient’s medical history was significant only for hypertension; he had not taken any antihypertensive or other medications for the past 3 days, as previously instructed by the EP at the other ED. The patient denied alcohol or drug abuse.

On physical examination, the patient’s vital signs were: temperature, 98.6°F; heart rate, 58 beats/minute; blood pressure, 130/90 mm Hg; and respiratory rate, 16 breaths/minute. Oxygen saturation was 100% on room air. Examination of the head was normal and without evidence of trauma. Both pupils measured 4 mm and were equally round and reactive to light; the patient’s extraocular movements were intact. The remainder of the head, eyes, ears, nose, and throat examination was normal. The neck was supple, without masses or meningeal signs. The cardiopulmonary and abdominal examinations were all normal. On neurological examination, the patient was awake, alert, and oriented to person, place, and time. Cranial nerves II through XII were intact, and the patient had 5/5 motor strength in all four extremities and a normal gait.

 

 

 

Because we were concerned about the patient’s unexplained syncopal episode, we ordered laboratory tests, including a complete blood count (CBC), evaluation of electrolytes and glucose levels, and kidney function. In addition, we also ordered an electrocardiogram (ECG) and a noncontrast computed tomography (CT) scan of the head. All laboratory test results were within normal range. The ECG, however, demonstrated sinus bradycardia (approximately 58 beats/minute), a normal PR and QRS interval, a normal axis, and an incomplete right bundle branch block with tall, large, splayed upright T waves in the precordial leads (Figure). Based on the abnormal ECG results, we ordered serum cardiac marker studies, the values of which were all within normal range. The noncontrast CT scan of the head revealed a low-density posterior fossa mass compressing the fourth ventricle with secondary hydrocephalus.

The patient was placed with his head in an upright position and given 1 g/kg mannitol and 10 mg dexamethasone intravenously (IV). Neurosurgery services were consulted, and the patient underwent surgery the following morning. Surgery confirmed the presence of a hemangioblastoma. The hemangioblastoma was successfully excised, and the patient had an uneventful recovery. Interestingly, the significant T-wave changes in the precordial leads were no longer present postoperatively.

Discussion

Syncope and near-syncope are common reasons for ED visits. Syncope is a syndrome characterized by a transient, self-limited episode of loss of consciousness occurring as a result of a brief interruption of the oxygen supply to the brain.1 This interruption is almost always due to a transient cessation of blood flow.1 In true syncope (as opposed to seizures or hypoglycemia), the episode is characterized by a rapid onset of loss of consciousness—with or without warning symptoms.1 It is important to determine the cause of syncope, because 7% to 23% of such patients will suffer serious outcomes within 7 to 30 days of their ED visit—either within a hospital setting or at home.2

Etiology

There are many causes of syncope. In most cases, the etiology falls under one of three broad categories: neurally mediated (or reflex mediated), orthostatic hypotensive-mediated, or cardiovascular (CV)-mediated. Less common causes of syncope include cerebrovascular injury.1 The Table outlines both common and uncommon causes of syncope.

 

 

 

On presentation, our patient had several possible causes for his syncopal episode: an abnormal ECG (CV); multiple episodes of emesis (volume depletion); and headache (cerebrovascular). The EP worked up all three of these signs and symptoms simultaneously as is the appropriate protocol when evaluating an ED patient presenting with undifferentiated syncope.

Signs and Symptoms

Patients with undiagnosed brain tumors normally present with headache, seizures, nausea, vomiting, focal neurological deficits, or an altered mental status.3 Syncope is a very rare manifestation of a brain tumor3; however, our patient did complain of headache, nausea, and vomiting.

In addition to the unusual cause of the syncope, the abnormally large upright T waves make this case even more notable. T-wave changes are the most common ECG abnormality, seen in about 50% of abnormal tracings reviewed in a hospital population and in 2.4% of all ECGs.4

In general, T-wave changes are a result of local changes in the duration of repolarization. T-wave inversion is the most common T-wave abnormality and is typically observed in the setting of ischemia, post-ingestion of food, following an episode of tachycardia or anxiety, and autonomic dysfunction.5 However, in patients who have a cerebral etiology (usually hemorrhage), the T-wave changes may be either upright (as in our case) or inverted.5 Historically, subarachnoid hemorrhage (SAH) has been associated with ST-segment elevation and T-wave inversion. Hypothalamic stimulation and autonomic dysfunction have been linked to abnormal T-waves, but this has not been conclusively proven to be the cause of the abnormality.6 For all of the aforementioned reasons, the specificity for a given cause of T-wave changes is exceedingly low.5

Hyperacute T-wave amplitude, with prominent symmetrical T waves in at least two continuous leads, may be the earliest sign of acute transmural myocardial infarction (MI).7 It usually persists for only a brief time before other ECG findings of acute MI are observed. Other common causes of hyperacute T waves include hyperkalemia (usually narrow-based, and peaked), early repolarization, left ventricular hypertrophy, and acute myocarditis.8 Less common causes of prominent T waves include pre-excitation  syndromes, pericarditis, and scorpion stings.9,10

Summary

It is unclear why our patient, who had a hemangioblastoma, demonstrated hyperacute T-wave abnormality on ECG. The abnormal upright T waves may have occurred secondary to the same theories regarding SAH, hypothalamic stimulation, or autonomic dysfunction. Regardless of the underlying etiology, this case serves as a reminder to the EP that not all T-wave changes on ECG are cardiac in origin. 

Case

A 34-year-old man presented to our ED via emergency medical services (EMS) following a syncopal episode. The patient stated that as he was getting ready for work earlier that morning, he experienced sudden lightheadedness and passed out, whereupon his wife immediately called EMS. The patient denied any previous history of syncope, but said he had been experiencing frequent episodes of nausea and vomiting over the past week. He also complained of a mild occipital headache that acetaminophen had failed to relieve.

The patient had been seen at a different ED 3 days earlier for nausea and vomiting. After evaluating the patient, the emergency physician (EP) at this facility felt the most likely cause of the patient’s gastrointestinal issues was related to hydralazine, his antihypertensive medication, and advised the patient to discontinue its use.

During evaluation at our ED, the patient denied fever, chills, neck stiffness, numbness, weakness, tingling of the extremities, or difficulty walking. He also denied chest pain, shortness of breath, or urinary symptoms. The patient’s medical history was significant only for hypertension; he had not taken any antihypertensive or other medications for the past 3 days, as previously instructed by the EP at the other ED. The patient denied alcohol or drug abuse.

On physical examination, the patient’s vital signs were: temperature, 98.6°F; heart rate, 58 beats/minute; blood pressure, 130/90 mm Hg; and respiratory rate, 16 breaths/minute. Oxygen saturation was 100% on room air. Examination of the head was normal and without evidence of trauma. Both pupils measured 4 mm and were equally round and reactive to light; the patient’s extraocular movements were intact. The remainder of the head, eyes, ears, nose, and throat examination was normal. The neck was supple, without masses or meningeal signs. The cardiopulmonary and abdominal examinations were all normal. On neurological examination, the patient was awake, alert, and oriented to person, place, and time. Cranial nerves II through XII were intact, and the patient had 5/5 motor strength in all four extremities and a normal gait.

 

 

 

Because we were concerned about the patient’s unexplained syncopal episode, we ordered laboratory tests, including a complete blood count (CBC), evaluation of electrolytes and glucose levels, and kidney function. In addition, we also ordered an electrocardiogram (ECG) and a noncontrast computed tomography (CT) scan of the head. All laboratory test results were within normal range. The ECG, however, demonstrated sinus bradycardia (approximately 58 beats/minute), a normal PR and QRS interval, a normal axis, and an incomplete right bundle branch block with tall, large, splayed upright T waves in the precordial leads (Figure). Based on the abnormal ECG results, we ordered serum cardiac marker studies, the values of which were all within normal range. The noncontrast CT scan of the head revealed a low-density posterior fossa mass compressing the fourth ventricle with secondary hydrocephalus.

The patient was placed with his head in an upright position and given 1 g/kg mannitol and 10 mg dexamethasone intravenously (IV). Neurosurgery services were consulted, and the patient underwent surgery the following morning. Surgery confirmed the presence of a hemangioblastoma. The hemangioblastoma was successfully excised, and the patient had an uneventful recovery. Interestingly, the significant T-wave changes in the precordial leads were no longer present postoperatively.

Discussion

Syncope and near-syncope are common reasons for ED visits. Syncope is a syndrome characterized by a transient, self-limited episode of loss of consciousness occurring as a result of a brief interruption of the oxygen supply to the brain.1 This interruption is almost always due to a transient cessation of blood flow.1 In true syncope (as opposed to seizures or hypoglycemia), the episode is characterized by a rapid onset of loss of consciousness—with or without warning symptoms.1 It is important to determine the cause of syncope, because 7% to 23% of such patients will suffer serious outcomes within 7 to 30 days of their ED visit—either within a hospital setting or at home.2

Etiology

There are many causes of syncope. In most cases, the etiology falls under one of three broad categories: neurally mediated (or reflex mediated), orthostatic hypotensive-mediated, or cardiovascular (CV)-mediated. Less common causes of syncope include cerebrovascular injury.1 The Table outlines both common and uncommon causes of syncope.

 

 

 

On presentation, our patient had several possible causes for his syncopal episode: an abnormal ECG (CV); multiple episodes of emesis (volume depletion); and headache (cerebrovascular). The EP worked up all three of these signs and symptoms simultaneously as is the appropriate protocol when evaluating an ED patient presenting with undifferentiated syncope.

Signs and Symptoms

Patients with undiagnosed brain tumors normally present with headache, seizures, nausea, vomiting, focal neurological deficits, or an altered mental status.3 Syncope is a very rare manifestation of a brain tumor3; however, our patient did complain of headache, nausea, and vomiting.

In addition to the unusual cause of the syncope, the abnormally large upright T waves make this case even more notable. T-wave changes are the most common ECG abnormality, seen in about 50% of abnormal tracings reviewed in a hospital population and in 2.4% of all ECGs.4

In general, T-wave changes are a result of local changes in the duration of repolarization. T-wave inversion is the most common T-wave abnormality and is typically observed in the setting of ischemia, post-ingestion of food, following an episode of tachycardia or anxiety, and autonomic dysfunction.5 However, in patients who have a cerebral etiology (usually hemorrhage), the T-wave changes may be either upright (as in our case) or inverted.5 Historically, subarachnoid hemorrhage (SAH) has been associated with ST-segment elevation and T-wave inversion. Hypothalamic stimulation and autonomic dysfunction have been linked to abnormal T-waves, but this has not been conclusively proven to be the cause of the abnormality.6 For all of the aforementioned reasons, the specificity for a given cause of T-wave changes is exceedingly low.5

Hyperacute T-wave amplitude, with prominent symmetrical T waves in at least two continuous leads, may be the earliest sign of acute transmural myocardial infarction (MI).7 It usually persists for only a brief time before other ECG findings of acute MI are observed. Other common causes of hyperacute T waves include hyperkalemia (usually narrow-based, and peaked), early repolarization, left ventricular hypertrophy, and acute myocarditis.8 Less common causes of prominent T waves include pre-excitation  syndromes, pericarditis, and scorpion stings.9,10

Summary

It is unclear why our patient, who had a hemangioblastoma, demonstrated hyperacute T-wave abnormality on ECG. The abnormal upright T waves may have occurred secondary to the same theories regarding SAH, hypothalamic stimulation, or autonomic dysfunction. Regardless of the underlying etiology, this case serves as a reminder to the EP that not all T-wave changes on ECG are cardiac in origin. 

References

1.    Puppala VK, Dickinson O, Benditt DG. Syncope: classification and risk stratification. J Cardiol. 2014;63(3):171-177.

2.    Thiruganasambandamoorthy V, Stiell IG, Sivilotti ML, et al. Risk stratification of adult emergency department syncope patients to predict short-term serious outcomes after discharge (RiSEDS) study. BMC Emerg Med. 2014;14(1):8.

3.    van der Sluijs BM, Renier WO, Kappelle AC. Brain tumor as a rare cause of cardiac syncope. J Neurooncol. 2004;67(1-2):241-244.

4.    Friedberg CK, Zagar A. Nonspecific ST and T-wave changes. Circulation. 1961;23:665-661.

5.    Fisch C. T wave abnormalities due to extracardiac “functional” causes. ACC Curr J Rev. 1997;6(2):101-104.

6.    Chatterjee S. ECG changes in subarachnoid hemorrhage: a synopsis. Neth Heart J. 2011;19(1):31-47.

7.    Vojáčeka, J, Janskýb P, Janotac T. Third universal definition of myocardial infarction. Cor Vasa. 2013;55:e228-e235.

8.    Levis JT. ECG diagnosis: hyperacute T waves. Perm J. 2015;19(3):79.

9.    Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002;20(3):243-251.

10.   Kumar MR, Bharath RV, Subrahmanyam BV, Rammohan P, Agrawal A. Scorpion envenomation and its management in adults. Sahel Med J. 2013;16(2):60-63.

References

1.    Puppala VK, Dickinson O, Benditt DG. Syncope: classification and risk stratification. J Cardiol. 2014;63(3):171-177.

2.    Thiruganasambandamoorthy V, Stiell IG, Sivilotti ML, et al. Risk stratification of adult emergency department syncope patients to predict short-term serious outcomes after discharge (RiSEDS) study. BMC Emerg Med. 2014;14(1):8.

3.    van der Sluijs BM, Renier WO, Kappelle AC. Brain tumor as a rare cause of cardiac syncope. J Neurooncol. 2004;67(1-2):241-244.

4.    Friedberg CK, Zagar A. Nonspecific ST and T-wave changes. Circulation. 1961;23:665-661.

5.    Fisch C. T wave abnormalities due to extracardiac “functional” causes. ACC Curr J Rev. 1997;6(2):101-104.

6.    Chatterjee S. ECG changes in subarachnoid hemorrhage: a synopsis. Neth Heart J. 2011;19(1):31-47.

7.    Vojáčeka, J, Janskýb P, Janotac T. Third universal definition of myocardial infarction. Cor Vasa. 2013;55:e228-e235.

8.    Levis JT. ECG diagnosis: hyperacute T waves. Perm J. 2015;19(3):79.

9.    Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002;20(3):243-251.

10.   Kumar MR, Bharath RV, Subrahmanyam BV, Rammohan P, Agrawal A. Scorpion envenomation and its management in adults. Sahel Med J. 2013;16(2):60-63.

Issue
Emergency Medicine - 48(8)
Issue
Emergency Medicine - 48(8)
Page Number
364-366
Page Number
364-366
Publications
Emergency Medicine
MDedge Emergency Medicine
Publications
Emergency Medicine
MDedge Emergency Medicine
Article Type
Article
Display Headline
An Unusual Cause of Syncope With T-Wave Abnormalities
Display Headline
An Unusual Cause of Syncope With T-Wave Abnormalities
Legacy Keywords
case report, syncope, t-wave, abnormalities, headache, case
Legacy Keywords
case report, syncope, t-wave, abnormalities, headache, case
Sections
Case Reports
Article Source

PURLs Copyright

Inside the Article

Teaser Media
Article PDF Media

High-Altitude Illness

Article Type
Article
Changed
Wed, 12/12/2018 - 20:10
Display Headline
High-Altitude Illness
Preventive measures, along with prompt recognition and treatment of altitude-related illness, are essential to improving outcomes and preventing life-threatening sequelae
Author(s)
Mischa Haroutunian, MD
Michael J. Bono, MD

Patients participating in occupational and sports-related activities requiring ascent to high elevations are at risk of developing a range of high-altitude illnesses. Prompt recognition and treatment are paramount to improving outcomes and preventing life-threatening sequelae. High-elevation locations are the setting of many recreational activities for outdoor enthusiasts. As such, illnesses associated with high altitude may be encountered by those summiting peaks, traveling by air, or working in flight medicine or as part of an emergency rescue team. The altitude syndromes discussed in this review are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). While these conditions do not represent all altitude-related illnesses, they are the primary pathological processes for which physicians should be familiar when working with high-altitude populations.

Physiological Response to Altitude

A knowledge of the physiological response to altitude helps to understand altitude-related illness. The normal acclimatization response to high elevation involves an increase in alveolar ventilation, referred to as hypoxic ventilatory response (HVR). The HVR is initiated by the carotid body, which acts as a peripheral chemosensor. Over the first 2 weeks at elevation, an increased sensitivity to hypoxia leads to a rise in ventilation. This precipitates an increase in alveolar oxygen pressure and arterial oxygen concentration, and a decrease in arterial carbon dioxide. Cardiac output increases, ventilation perfusion-matching is improved, and pulmonary arterial pressure rises. Respiratory alkalosis develops secondary to this hyperventilation; as a compensatory response, increased excretion of bicarbonate by the kidneys occurs, leading to a normalization of pH, which peaks at about 7 days. These physiological changes result in hyperventilation, increased urinary output, periodic nighttime breathing, and dyspnea on exertion. Periodic nighttime breathing is characterized by periods of hyperpnea followed by apnea during sleep. The duration of apnea is commonly 3 to 10 seconds, but may last up to 15 seconds. These symptoms may be considered normal at elevations above 8,000 ft.

The Lake Louise Criteria
At the 1991 International Hypoxia Symposium in Alberta, Canada, the Lake Louise criteria regarding the diagnosis of altitude illness was developed and adopted.1 This consensus statement provides definitions for AMS, HACE, and HAPE (Table 1). In addition to the definition criteria, a self-assessment scoring system, which includes a clinical assessment, was developed to assist in diagnosing high-altitude illness (Table 2).2

Acute Mountain Sickness

Acute mountain sickness comprises a constellation of symptoms caused by the atmospheric changes at elevations above approximately 2,500 m. It is the most common form of high-altitude illness, affecting 25% of travelers at moderate altitude and 50% to 85% above 4,000 m.3

Symptoms
The onset of symptoms (eg, headache, anorexia, nausea, vomiting, weakness) may occur at 2,000 m in the setting of rapid ascent—most commonly at 6 to 12 hours, but onset can range from 1 hour to 2 days after ascent. If symptoms begin after 3 days, other diagnoses should be considered. Symptoms of AMS are generally worse after the first night of sleep at elevation. On physical examination, vital signs are usually normal, though postural hypotension and tachycardia are possible. Oxygen saturation may be markedly decreased after rapid ascent, and chest auscultation may reveal rales in 20% of patients.4 Peripheral and facial edema may also be present. Funduscopic examination may show venous tortuosity and dilation, and retinal hemorrhage is common in ascents over 4,800 m.

© Shutterstock/sezer66
    

Differential Diagnosis
The differential diagnosis for AMS is broad and includes hypothermia, dehydration, exhaustion, subarachnoid hemorrhage, intracranial mass, carbon monoxide poisoning, alcohol hangover, intoxication, central nervous system infection and migraine. Risk factors for developing AMS are a previous history of altitude illness, rapid ascent, and lack of previous acclimatization. Interestingly, physical fitness does not protect a person from developing AMS.5

Mechanism of AMS
The true mechanism of AMS is uncertain, but it is clear that a fall in barometric pressure results in hypobaric hypoxia. This is thought to lead to an increased blood volume in the brain and increased cerebral blood flow, possibly precipitating an enlarged brain. A mechanism related to vasogenic edema has been proposed due to patients’ clinical improvement with dexamethasone therapy.6 Acute mountain sickness does appear to be related to overall fluid balance, as an increase in reninangiotensin, aldosterone, and antidiuretic hormone has been observed in patients with the condition. Elevation of these hormones is contrary to the appropriate physiological response of diuresis.

Treatment
Treatment of AMS begins with descent from elevation as soon as possible. Descent should be at least 500 m from the aggravating elevation. Patients should remain at least 1 to 2 days at this lower elevation before attempting reascent. If descent is not feasible, any further ascent should be delayed until symptoms have resolved.
     Dexamethasone. This glucocorticoid has been used clinically with good success, although the mechanism of action in unclear. The initial dose is 8 mg followed by 4 mg every 6 hours.3
     Acetazolamide. A carbonic anhydrase inhibitor, acetazolamide acts to temper symptoms by causing an acidosis that increases ventilation and prevents periodic breathing and hypoxia during sleep. The standard dose is 250 mg twice daily.3
    Oxygen. Supplemental oxygen provided at 1 to 2 L/min via nasal cannula for 12 to 24 hours may help to improve symptoms. A portable hyperbaric oxygen (HBO) bag (eg, a Gamow bag) can be used to create an effective altitude of approximately 1,500 to 2,000 m inside the bag. The patient is placed completely within the bag, the zipper is sealed shut, and the bag is inflated with a foot pump. Treatment in such a chamber can be provided in 1-hour increments and repeated as needed. However, if descent is possible, use of the HBO chamber should not prevent or delay descent.
     Ibuprofen. Compared to placebo, studies have shown ibuprofen 600 mg three times a day reduces the severity of AMS.7

Prevention
Strategies to prevent AMS are similar to those used to treat the condition. These include gradual ascent and prophylactic drug therapy.
     Gradual Ascent. Gradual ascent is the primary strategy to prevent AMS. At altitudes above 3,000 m, each subsequent night should not be spent at an elevation 300 m higher than the previous night.
     Acetazolamide. Pretreatment with acetazolamide is indicated for patients with a history of altitude illness or who anticipate an abrupt ascent (eg, rescue workers). Acetazolamide has been shown in multiple studies to be effective in the prevention of AMS.8 Adverse side effects of acetazolamide include paresthesias and increased urinary frequency; the drug may also make carbonated beverages taste flat. The preventive dose is 125 mg twice daily, and should be started the day before ascent.
     Dexamethasone. In addition to treating AMS, dexamethasone may be taken as a preventive in doses of 2 mg every 6 hours or 4 mg twice daily.3 However, unlike acetazolamide, which acts to facilitate acclimatization, dexamethasone only prevents symptoms. Thus, cessation of the drug can result in rebound AMS symptoms, and prolonged use can result in adrenal suppression.3 Therefore, it should not be used for more than 10 days.
     Sumatriptan and Gabapentin. In recent studies, sumatriptan and gabapentin haven shown benefit in preventing AMS, 9,10 but further study is needed before either of these drugs can be recommended.
     Ginkgo Biloba. While ginkgo biloba has been touted as an effective preventive treatment, studies have shown no benefit to its use.8
    Ibuprofen. ibuprofen 600 mg three times daily can be initiated the day prior to ascent, and has been shown to decrease the incidence of AMS.7

 

 

High-Altitude Cerebral Edema

High-altitude cerebral edema, a condition that can be considered on a continuum with AMS, is hallmarked by progressive neurological symptoms. It is defined by either the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status changes and ataxia in a person without AMS. Clinical signs are truncal ataxia, hallucinations, confusion, vomiting, decreased activity, mild fever, upper motor neuronal signs, stupor, or coma.5 Development of HACE usually requires at least 2 days of altitudes above 4000 m.5

Mechanism of HACE
The exact mechanism of HACE is unclear. Magnetic resonance imaging of patients with the condition demonstrates cerebral edema primarily localized to the corpus callosum.11 These findings suggest an increased permeability in the blood-brain barrier, leading to vasogenic cerebral edema. Cases of death associated with HACE are the result of herniation. Fortunately, if the condition is recognized promptly and appropriate management is instituted, most patients will recover without permanent deficits.

Treatment
Current recommendations for treating HACE are similar to treatment strategies for AMS.
    Descent. A therapeutic priority, descent may prove challenging as the patient may be ataxic, have altered mental status, and have difficulty facilitating his or her own descent.
     Oxygen. A portable HBO bag can be used to simulate descent until evacuation is possible. Supplemental oxygen should be applied immediately.
    Dexamethasone. In treating HACE, dexamethasone may be administered at a loading dose of 8 mg, followed by 4 mg every 6 hours.3
     Airway Management. If the patient has significantly altered mental status, appropriate airway management must be initiated.

High-Altitude Pulmonary Edema

The most common cause of death from altitude illness is HAPE,12 a form of noncardiogenic pulmonary edema. This condition generally occurs at elevations above 3,000 m. Symptoms begin 2 to 5 days after ascent and progress in a typical pattern. A patient will initially experience a nonproductive cough and dyspnea at rest. The dyspnea worsens, and the cough becomes productive of pink, frothy sputum. Without medical intervention, lethargy, coma, and death may follow.

Symptoms of HAPE generally worsen following a night of sleep at elevation. Physical examination reveals crackles, tachycardia, tachypnea, and hypoxia. Diagnosis requires at least two of the following signs:

  • Crackles or wheezing in at least one lung field
  • Central cyanosis
  • Tachypnea
  • Tachycardia.

In addition to the above signs, at least two of the following symptoms must also be present:

  • Dyspnea at rest
  • Cough
  • Weakness or decreased exercise performance
  • Chest tightness
  • Congestion.

Chest X-ray typically reveals patchy opacities at varying locations (Figure 2). There are often infiltrates in the right middle lobe. Ultrasound has been used to facilitate the diagnosis of HAPE in the field.13 The “comet-tail” sign is a term used to describe echogenic patterns in the lung as a result of increased lymphatic flow (Figure 3). This sign, if seen in the clinical setting of HAPE, may aid in the diagnosis and monitoring of treatment efficacy.13

Mechanism of HAPE
The mechanism of HAPE is better understood than that of AMS and HACE. In HAPE, high microvascular pressures in the lungs lead to elevated pulmonary vascular resistance and pulmonary artery pressure. Pulmonary edema ensues, but left ventricular function is preserved. Patients with a naturally low HVR, high pulmonary artery pressures at rest, preexisting pulmonary hypertension, or a previous history of HAPE are predisposed to developing the condition. Risk factors include heavy exertion, rapid ascent, cold, salt ingestion, and sleeping medications.

© Shutterstock/Telegin Sergey
    

Treatment
Decent and warming of the patient as soon as possible, along with treatment outlined below, are essential.
     Oxygen. Treatment of HAPE begins with supplemental oxygen to immediately lower pulmonary artery pressure. Oxygen should initially be administered at 4 to 6 L/min; if the patient improves clinically and can maintain oxygen saturations greater than 90%, oxygen may be decreased with a goal to maintain saturation above 90%.
     Nifedipine. Following oxygen, descent, and warming, nifedipine can be used as an adjunctive therapy. The treatment dose for HAPE is 20 to 30 mg of the sustained release form every 12 hours.3
     Salmeterol/Albuterol and Expiratory Positive Airway Pressure. The oral inhalers salmeterol or albuterol may be used for bronchodilation; however, there is little evidence to support their effectiveness in HAPE. Ventilation with expiratory positive airway pressure can be employed if available.

Prevention
For patients with a predisposition to HAPE, preventive measures should be considered prior to ascent. As with all forms of altitude illness, gradual ascent is the most effective prevention method available.
     Phosphodiesterase Inhibitors. Phosphodiesterase inhibitors act via pulmonary vasodilation to prevent HAPE in some patients. Tadalafil at a dose of 10 mg twice daily or 20 mg once daily has been shown to reduce the incidence of HAPE.14 Alternatively, sildenafil 50 mg three times daily may be used.
     Acetazolamide and β-Agonists. Although both acetazolamide and β-agonists such as albuterol have been theorized to aid in preventing HAPE, this has not been proven.15

 

 

Conclusion

Clinically, high-altitude illnesses range from subtle symptoms to severe, life threatening disease. Knowledge of these disease processes and clinical presentation prior to travel or work in a high-altitude setting is essential. Rapid recognition of symptoms and prompt, appropriate interventions, such as descent when necessary, can significantly improve the outcomes of these conditions.

Dr Haroutunian is an emergency physician, department of emergency medicine, Exempla St Joseph Hospital, Denver, Colorado. Dr Bono is professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

References

  1. Hackett PH, Oelz O. The Lake Louise consensus on the definition and qualification of altitude illness. In: Sutton JR, Coates G, Houston CS, eds. Hypoxia and Mountain Medicine. Burlington, VT: Queen City Printers; 1992:327-330.
  2. Roach RC, Bärtch P, Hackett PH, Oelz O, and the Lake Louise AMS Scoring Consensus Committee. The Lake Louise Acute Mountain Sickness Scoring System. In: Hypoxia and Molecular Medicine. Proceedings of the 8th International Hypoxia Symposium. Burlington, VT: Queen City Printers; 1993:272-274.
  3. Eide RP 3rd, Asplund CA. Altitude illness: update on prevention and treatment. Curr Sports Med Rep. 2012;11(3):124-130.
  4. Milzman DP, Damergis JA, Napoli AM. Rapid ascent changes in vitals at altitude. Ann Emerg Med. 2008;51(4):536.
  5. Bärtsch P, Swenson ER. Clinical practice: Acute high-altitude illnesses. N Engl J Med. 2013;368(24):2294-2302.
  6. Hackett PH, Roach RC. Medical therapy of mountain illness. Ann Emerg Med. 1987;16(9):980-986.
  7. Lipman GS, Kanaan NC, Holck PS, Constance BB, Gertsch JH; PAINS Group. Ibuprofen prevents altitude illness: a randomized controlled trial for prevention of altitude illness with nonsteroidal anti-inflammatories. Ann Emerg Med. 2012;59(6): 484-490.
  8. Seupaul RA, Welch JL, Malka ST, Emmett TW. Pharmacologic prophylaxis for acute mountain sickness: a systematic shortcut review. Ann Emerg Med. 2012; 59(4):307-317.
  9. Jafarian S, Gorouhi F, Salimi S, Lotfi J. Sumatriptan for prevention of acute mountain sickness: randomized clinical trial. Ann Neurol. 2007;62(3):273-277.
  10. Jafarian S, Abolfazli R, Gorouhi F, Rezaie S, Lotfi J. Gabapentin for prevention of hypobaric hypoxia-induced headache: randomized double-blind clinical trial. J Neurol Neurosurg Psychiatry. 2008;79(3): 321-323.
  11. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280(22):1920-1925.
  12. Gallagher SA1, Hackett PH. High-altitude illness. Emerg Med Clin North Am. 2004;22(2):329-355.
  13. Fagenholz PJ, Gutman JA, Murray AF, Noble VE, Thomas SH, Harris NS. Chest ultrasonography for the diagnosis and monitoring of high-altitude pulmonary edema. Chest. 2007;131(4): 1013-1018.
  14. Leshem E1, Caine Y, Rosenberg E, Maaravi Y, Hermesh H, Schwartz E. Tadalafil and acetazolamide versus acetazolamide for the prevention of severe high-altitude illness. J Travel Med. 2012;19(5): 308-310.
  15. Schoene RB. Illnesses at high altitude. Chest. 2008;134(2):402-416.
Author and Disclosure Information

Issue
Emergency Medicine - 46(5)
Publications
Emergency Medicine
MDedge Emergency Medicine
Topics
Sports Medicine
Imaging
Mental Health
Cardiology
Pulmonology
Page Number
202-210
Author(s)
Mischa Haroutunian, MD
Michael J. Bono, MD
Author(s)
Mischa Haroutunian, MD
Michael J. Bono, MD
Author and Disclosure Information

Author and Disclosure Information

Preventive measures, along with prompt recognition and treatment of altitude-related illness, are essential to improving outcomes and preventing life-threatening sequelae
Preventive measures, along with prompt recognition and treatment of altitude-related illness, are essential to improving outcomes and preventing life-threatening sequelae

Patients participating in occupational and sports-related activities requiring ascent to high elevations are at risk of developing a range of high-altitude illnesses. Prompt recognition and treatment are paramount to improving outcomes and preventing life-threatening sequelae. High-elevation locations are the setting of many recreational activities for outdoor enthusiasts. As such, illnesses associated with high altitude may be encountered by those summiting peaks, traveling by air, or working in flight medicine or as part of an emergency rescue team. The altitude syndromes discussed in this review are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). While these conditions do not represent all altitude-related illnesses, they are the primary pathological processes for which physicians should be familiar when working with high-altitude populations.

Physiological Response to Altitude

A knowledge of the physiological response to altitude helps to understand altitude-related illness. The normal acclimatization response to high elevation involves an increase in alveolar ventilation, referred to as hypoxic ventilatory response (HVR). The HVR is initiated by the carotid body, which acts as a peripheral chemosensor. Over the first 2 weeks at elevation, an increased sensitivity to hypoxia leads to a rise in ventilation. This precipitates an increase in alveolar oxygen pressure and arterial oxygen concentration, and a decrease in arterial carbon dioxide. Cardiac output increases, ventilation perfusion-matching is improved, and pulmonary arterial pressure rises. Respiratory alkalosis develops secondary to this hyperventilation; as a compensatory response, increased excretion of bicarbonate by the kidneys occurs, leading to a normalization of pH, which peaks at about 7 days. These physiological changes result in hyperventilation, increased urinary output, periodic nighttime breathing, and dyspnea on exertion. Periodic nighttime breathing is characterized by periods of hyperpnea followed by apnea during sleep. The duration of apnea is commonly 3 to 10 seconds, but may last up to 15 seconds. These symptoms may be considered normal at elevations above 8,000 ft.

The Lake Louise Criteria
At the 1991 International Hypoxia Symposium in Alberta, Canada, the Lake Louise criteria regarding the diagnosis of altitude illness was developed and adopted.1 This consensus statement provides definitions for AMS, HACE, and HAPE (Table 1). In addition to the definition criteria, a self-assessment scoring system, which includes a clinical assessment, was developed to assist in diagnosing high-altitude illness (Table 2).2

Acute Mountain Sickness

Acute mountain sickness comprises a constellation of symptoms caused by the atmospheric changes at elevations above approximately 2,500 m. It is the most common form of high-altitude illness, affecting 25% of travelers at moderate altitude and 50% to 85% above 4,000 m.3

Symptoms
The onset of symptoms (eg, headache, anorexia, nausea, vomiting, weakness) may occur at 2,000 m in the setting of rapid ascent—most commonly at 6 to 12 hours, but onset can range from 1 hour to 2 days after ascent. If symptoms begin after 3 days, other diagnoses should be considered. Symptoms of AMS are generally worse after the first night of sleep at elevation. On physical examination, vital signs are usually normal, though postural hypotension and tachycardia are possible. Oxygen saturation may be markedly decreased after rapid ascent, and chest auscultation may reveal rales in 20% of patients.4 Peripheral and facial edema may also be present. Funduscopic examination may show venous tortuosity and dilation, and retinal hemorrhage is common in ascents over 4,800 m.

© Shutterstock/sezer66
    

Differential Diagnosis
The differential diagnosis for AMS is broad and includes hypothermia, dehydration, exhaustion, subarachnoid hemorrhage, intracranial mass, carbon monoxide poisoning, alcohol hangover, intoxication, central nervous system infection and migraine. Risk factors for developing AMS are a previous history of altitude illness, rapid ascent, and lack of previous acclimatization. Interestingly, physical fitness does not protect a person from developing AMS.5

Mechanism of AMS
The true mechanism of AMS is uncertain, but it is clear that a fall in barometric pressure results in hypobaric hypoxia. This is thought to lead to an increased blood volume in the brain and increased cerebral blood flow, possibly precipitating an enlarged brain. A mechanism related to vasogenic edema has been proposed due to patients’ clinical improvement with dexamethasone therapy.6 Acute mountain sickness does appear to be related to overall fluid balance, as an increase in reninangiotensin, aldosterone, and antidiuretic hormone has been observed in patients with the condition. Elevation of these hormones is contrary to the appropriate physiological response of diuresis.

Treatment
Treatment of AMS begins with descent from elevation as soon as possible. Descent should be at least 500 m from the aggravating elevation. Patients should remain at least 1 to 2 days at this lower elevation before attempting reascent. If descent is not feasible, any further ascent should be delayed until symptoms have resolved.
     Dexamethasone. This glucocorticoid has been used clinically with good success, although the mechanism of action in unclear. The initial dose is 8 mg followed by 4 mg every 6 hours.3
     Acetazolamide. A carbonic anhydrase inhibitor, acetazolamide acts to temper symptoms by causing an acidosis that increases ventilation and prevents periodic breathing and hypoxia during sleep. The standard dose is 250 mg twice daily.3
    Oxygen. Supplemental oxygen provided at 1 to 2 L/min via nasal cannula for 12 to 24 hours may help to improve symptoms. A portable hyperbaric oxygen (HBO) bag (eg, a Gamow bag) can be used to create an effective altitude of approximately 1,500 to 2,000 m inside the bag. The patient is placed completely within the bag, the zipper is sealed shut, and the bag is inflated with a foot pump. Treatment in such a chamber can be provided in 1-hour increments and repeated as needed. However, if descent is possible, use of the HBO chamber should not prevent or delay descent.
     Ibuprofen. Compared to placebo, studies have shown ibuprofen 600 mg three times a day reduces the severity of AMS.7

Prevention
Strategies to prevent AMS are similar to those used to treat the condition. These include gradual ascent and prophylactic drug therapy.
     Gradual Ascent. Gradual ascent is the primary strategy to prevent AMS. At altitudes above 3,000 m, each subsequent night should not be spent at an elevation 300 m higher than the previous night.
     Acetazolamide. Pretreatment with acetazolamide is indicated for patients with a history of altitude illness or who anticipate an abrupt ascent (eg, rescue workers). Acetazolamide has been shown in multiple studies to be effective in the prevention of AMS.8 Adverse side effects of acetazolamide include paresthesias and increased urinary frequency; the drug may also make carbonated beverages taste flat. The preventive dose is 125 mg twice daily, and should be started the day before ascent.
     Dexamethasone. In addition to treating AMS, dexamethasone may be taken as a preventive in doses of 2 mg every 6 hours or 4 mg twice daily.3 However, unlike acetazolamide, which acts to facilitate acclimatization, dexamethasone only prevents symptoms. Thus, cessation of the drug can result in rebound AMS symptoms, and prolonged use can result in adrenal suppression.3 Therefore, it should not be used for more than 10 days.
     Sumatriptan and Gabapentin. In recent studies, sumatriptan and gabapentin haven shown benefit in preventing AMS, 9,10 but further study is needed before either of these drugs can be recommended.
     Ginkgo Biloba. While ginkgo biloba has been touted as an effective preventive treatment, studies have shown no benefit to its use.8
    Ibuprofen. ibuprofen 600 mg three times daily can be initiated the day prior to ascent, and has been shown to decrease the incidence of AMS.7

 

 

High-Altitude Cerebral Edema

High-altitude cerebral edema, a condition that can be considered on a continuum with AMS, is hallmarked by progressive neurological symptoms. It is defined by either the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status changes and ataxia in a person without AMS. Clinical signs are truncal ataxia, hallucinations, confusion, vomiting, decreased activity, mild fever, upper motor neuronal signs, stupor, or coma.5 Development of HACE usually requires at least 2 days of altitudes above 4000 m.5

Mechanism of HACE
The exact mechanism of HACE is unclear. Magnetic resonance imaging of patients with the condition demonstrates cerebral edema primarily localized to the corpus callosum.11 These findings suggest an increased permeability in the blood-brain barrier, leading to vasogenic cerebral edema. Cases of death associated with HACE are the result of herniation. Fortunately, if the condition is recognized promptly and appropriate management is instituted, most patients will recover without permanent deficits.

Treatment
Current recommendations for treating HACE are similar to treatment strategies for AMS.
    Descent. A therapeutic priority, descent may prove challenging as the patient may be ataxic, have altered mental status, and have difficulty facilitating his or her own descent.
     Oxygen. A portable HBO bag can be used to simulate descent until evacuation is possible. Supplemental oxygen should be applied immediately.
    Dexamethasone. In treating HACE, dexamethasone may be administered at a loading dose of 8 mg, followed by 4 mg every 6 hours.3
     Airway Management. If the patient has significantly altered mental status, appropriate airway management must be initiated.

High-Altitude Pulmonary Edema

The most common cause of death from altitude illness is HAPE,12 a form of noncardiogenic pulmonary edema. This condition generally occurs at elevations above 3,000 m. Symptoms begin 2 to 5 days after ascent and progress in a typical pattern. A patient will initially experience a nonproductive cough and dyspnea at rest. The dyspnea worsens, and the cough becomes productive of pink, frothy sputum. Without medical intervention, lethargy, coma, and death may follow.

Symptoms of HAPE generally worsen following a night of sleep at elevation. Physical examination reveals crackles, tachycardia, tachypnea, and hypoxia. Diagnosis requires at least two of the following signs:

  • Crackles or wheezing in at least one lung field
  • Central cyanosis
  • Tachypnea
  • Tachycardia.

In addition to the above signs, at least two of the following symptoms must also be present:

  • Dyspnea at rest
  • Cough
  • Weakness or decreased exercise performance
  • Chest tightness
  • Congestion.

Chest X-ray typically reveals patchy opacities at varying locations (Figure 2). There are often infiltrates in the right middle lobe. Ultrasound has been used to facilitate the diagnosis of HAPE in the field.13 The “comet-tail” sign is a term used to describe echogenic patterns in the lung as a result of increased lymphatic flow (Figure 3). This sign, if seen in the clinical setting of HAPE, may aid in the diagnosis and monitoring of treatment efficacy.13

Mechanism of HAPE
The mechanism of HAPE is better understood than that of AMS and HACE. In HAPE, high microvascular pressures in the lungs lead to elevated pulmonary vascular resistance and pulmonary artery pressure. Pulmonary edema ensues, but left ventricular function is preserved. Patients with a naturally low HVR, high pulmonary artery pressures at rest, preexisting pulmonary hypertension, or a previous history of HAPE are predisposed to developing the condition. Risk factors include heavy exertion, rapid ascent, cold, salt ingestion, and sleeping medications.

© Shutterstock/Telegin Sergey
    

Treatment
Decent and warming of the patient as soon as possible, along with treatment outlined below, are essential.
     Oxygen. Treatment of HAPE begins with supplemental oxygen to immediately lower pulmonary artery pressure. Oxygen should initially be administered at 4 to 6 L/min; if the patient improves clinically and can maintain oxygen saturations greater than 90%, oxygen may be decreased with a goal to maintain saturation above 90%.
     Nifedipine. Following oxygen, descent, and warming, nifedipine can be used as an adjunctive therapy. The treatment dose for HAPE is 20 to 30 mg of the sustained release form every 12 hours.3
     Salmeterol/Albuterol and Expiratory Positive Airway Pressure. The oral inhalers salmeterol or albuterol may be used for bronchodilation; however, there is little evidence to support their effectiveness in HAPE. Ventilation with expiratory positive airway pressure can be employed if available.

Prevention
For patients with a predisposition to HAPE, preventive measures should be considered prior to ascent. As with all forms of altitude illness, gradual ascent is the most effective prevention method available.
     Phosphodiesterase Inhibitors. Phosphodiesterase inhibitors act via pulmonary vasodilation to prevent HAPE in some patients. Tadalafil at a dose of 10 mg twice daily or 20 mg once daily has been shown to reduce the incidence of HAPE.14 Alternatively, sildenafil 50 mg three times daily may be used.
     Acetazolamide and β-Agonists. Although both acetazolamide and β-agonists such as albuterol have been theorized to aid in preventing HAPE, this has not been proven.15

 

 

Conclusion

Clinically, high-altitude illnesses range from subtle symptoms to severe, life threatening disease. Knowledge of these disease processes and clinical presentation prior to travel or work in a high-altitude setting is essential. Rapid recognition of symptoms and prompt, appropriate interventions, such as descent when necessary, can significantly improve the outcomes of these conditions.

Dr Haroutunian is an emergency physician, department of emergency medicine, Exempla St Joseph Hospital, Denver, Colorado. Dr Bono is professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

Patients participating in occupational and sports-related activities requiring ascent to high elevations are at risk of developing a range of high-altitude illnesses. Prompt recognition and treatment are paramount to improving outcomes and preventing life-threatening sequelae. High-elevation locations are the setting of many recreational activities for outdoor enthusiasts. As such, illnesses associated with high altitude may be encountered by those summiting peaks, traveling by air, or working in flight medicine or as part of an emergency rescue team. The altitude syndromes discussed in this review are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). While these conditions do not represent all altitude-related illnesses, they are the primary pathological processes for which physicians should be familiar when working with high-altitude populations.

Physiological Response to Altitude

A knowledge of the physiological response to altitude helps to understand altitude-related illness. The normal acclimatization response to high elevation involves an increase in alveolar ventilation, referred to as hypoxic ventilatory response (HVR). The HVR is initiated by the carotid body, which acts as a peripheral chemosensor. Over the first 2 weeks at elevation, an increased sensitivity to hypoxia leads to a rise in ventilation. This precipitates an increase in alveolar oxygen pressure and arterial oxygen concentration, and a decrease in arterial carbon dioxide. Cardiac output increases, ventilation perfusion-matching is improved, and pulmonary arterial pressure rises. Respiratory alkalosis develops secondary to this hyperventilation; as a compensatory response, increased excretion of bicarbonate by the kidneys occurs, leading to a normalization of pH, which peaks at about 7 days. These physiological changes result in hyperventilation, increased urinary output, periodic nighttime breathing, and dyspnea on exertion. Periodic nighttime breathing is characterized by periods of hyperpnea followed by apnea during sleep. The duration of apnea is commonly 3 to 10 seconds, but may last up to 15 seconds. These symptoms may be considered normal at elevations above 8,000 ft.

The Lake Louise Criteria
At the 1991 International Hypoxia Symposium in Alberta, Canada, the Lake Louise criteria regarding the diagnosis of altitude illness was developed and adopted.1 This consensus statement provides definitions for AMS, HACE, and HAPE (Table 1). In addition to the definition criteria, a self-assessment scoring system, which includes a clinical assessment, was developed to assist in diagnosing high-altitude illness (Table 2).2

Acute Mountain Sickness

Acute mountain sickness comprises a constellation of symptoms caused by the atmospheric changes at elevations above approximately 2,500 m. It is the most common form of high-altitude illness, affecting 25% of travelers at moderate altitude and 50% to 85% above 4,000 m.3

Symptoms
The onset of symptoms (eg, headache, anorexia, nausea, vomiting, weakness) may occur at 2,000 m in the setting of rapid ascent—most commonly at 6 to 12 hours, but onset can range from 1 hour to 2 days after ascent. If symptoms begin after 3 days, other diagnoses should be considered. Symptoms of AMS are generally worse after the first night of sleep at elevation. On physical examination, vital signs are usually normal, though postural hypotension and tachycardia are possible. Oxygen saturation may be markedly decreased after rapid ascent, and chest auscultation may reveal rales in 20% of patients.4 Peripheral and facial edema may also be present. Funduscopic examination may show venous tortuosity and dilation, and retinal hemorrhage is common in ascents over 4,800 m.

© Shutterstock/sezer66
    

Differential Diagnosis
The differential diagnosis for AMS is broad and includes hypothermia, dehydration, exhaustion, subarachnoid hemorrhage, intracranial mass, carbon monoxide poisoning, alcohol hangover, intoxication, central nervous system infection and migraine. Risk factors for developing AMS are a previous history of altitude illness, rapid ascent, and lack of previous acclimatization. Interestingly, physical fitness does not protect a person from developing AMS.5

Mechanism of AMS
The true mechanism of AMS is uncertain, but it is clear that a fall in barometric pressure results in hypobaric hypoxia. This is thought to lead to an increased blood volume in the brain and increased cerebral blood flow, possibly precipitating an enlarged brain. A mechanism related to vasogenic edema has been proposed due to patients’ clinical improvement with dexamethasone therapy.6 Acute mountain sickness does appear to be related to overall fluid balance, as an increase in reninangiotensin, aldosterone, and antidiuretic hormone has been observed in patients with the condition. Elevation of these hormones is contrary to the appropriate physiological response of diuresis.

Treatment
Treatment of AMS begins with descent from elevation as soon as possible. Descent should be at least 500 m from the aggravating elevation. Patients should remain at least 1 to 2 days at this lower elevation before attempting reascent. If descent is not feasible, any further ascent should be delayed until symptoms have resolved.
     Dexamethasone. This glucocorticoid has been used clinically with good success, although the mechanism of action in unclear. The initial dose is 8 mg followed by 4 mg every 6 hours.3
     Acetazolamide. A carbonic anhydrase inhibitor, acetazolamide acts to temper symptoms by causing an acidosis that increases ventilation and prevents periodic breathing and hypoxia during sleep. The standard dose is 250 mg twice daily.3
    Oxygen. Supplemental oxygen provided at 1 to 2 L/min via nasal cannula for 12 to 24 hours may help to improve symptoms. A portable hyperbaric oxygen (HBO) bag (eg, a Gamow bag) can be used to create an effective altitude of approximately 1,500 to 2,000 m inside the bag. The patient is placed completely within the bag, the zipper is sealed shut, and the bag is inflated with a foot pump. Treatment in such a chamber can be provided in 1-hour increments and repeated as needed. However, if descent is possible, use of the HBO chamber should not prevent or delay descent.
     Ibuprofen. Compared to placebo, studies have shown ibuprofen 600 mg three times a day reduces the severity of AMS.7

Prevention
Strategies to prevent AMS are similar to those used to treat the condition. These include gradual ascent and prophylactic drug therapy.
     Gradual Ascent. Gradual ascent is the primary strategy to prevent AMS. At altitudes above 3,000 m, each subsequent night should not be spent at an elevation 300 m higher than the previous night.
     Acetazolamide. Pretreatment with acetazolamide is indicated for patients with a history of altitude illness or who anticipate an abrupt ascent (eg, rescue workers). Acetazolamide has been shown in multiple studies to be effective in the prevention of AMS.8 Adverse side effects of acetazolamide include paresthesias and increased urinary frequency; the drug may also make carbonated beverages taste flat. The preventive dose is 125 mg twice daily, and should be started the day before ascent.
     Dexamethasone. In addition to treating AMS, dexamethasone may be taken as a preventive in doses of 2 mg every 6 hours or 4 mg twice daily.3 However, unlike acetazolamide, which acts to facilitate acclimatization, dexamethasone only prevents symptoms. Thus, cessation of the drug can result in rebound AMS symptoms, and prolonged use can result in adrenal suppression.3 Therefore, it should not be used for more than 10 days.
     Sumatriptan and Gabapentin. In recent studies, sumatriptan and gabapentin haven shown benefit in preventing AMS, 9,10 but further study is needed before either of these drugs can be recommended.
     Ginkgo Biloba. While ginkgo biloba has been touted as an effective preventive treatment, studies have shown no benefit to its use.8
    Ibuprofen. ibuprofen 600 mg three times daily can be initiated the day prior to ascent, and has been shown to decrease the incidence of AMS.7

 

 

High-Altitude Cerebral Edema

High-altitude cerebral edema, a condition that can be considered on a continuum with AMS, is hallmarked by progressive neurological symptoms. It is defined by either the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status changes and ataxia in a person without AMS. Clinical signs are truncal ataxia, hallucinations, confusion, vomiting, decreased activity, mild fever, upper motor neuronal signs, stupor, or coma.5 Development of HACE usually requires at least 2 days of altitudes above 4000 m.5

Mechanism of HACE
The exact mechanism of HACE is unclear. Magnetic resonance imaging of patients with the condition demonstrates cerebral edema primarily localized to the corpus callosum.11 These findings suggest an increased permeability in the blood-brain barrier, leading to vasogenic cerebral edema. Cases of death associated with HACE are the result of herniation. Fortunately, if the condition is recognized promptly and appropriate management is instituted, most patients will recover without permanent deficits.

Treatment
Current recommendations for treating HACE are similar to treatment strategies for AMS.
    Descent. A therapeutic priority, descent may prove challenging as the patient may be ataxic, have altered mental status, and have difficulty facilitating his or her own descent.
     Oxygen. A portable HBO bag can be used to simulate descent until evacuation is possible. Supplemental oxygen should be applied immediately.
    Dexamethasone. In treating HACE, dexamethasone may be administered at a loading dose of 8 mg, followed by 4 mg every 6 hours.3
     Airway Management. If the patient has significantly altered mental status, appropriate airway management must be initiated.

High-Altitude Pulmonary Edema

The most common cause of death from altitude illness is HAPE,12 a form of noncardiogenic pulmonary edema. This condition generally occurs at elevations above 3,000 m. Symptoms begin 2 to 5 days after ascent and progress in a typical pattern. A patient will initially experience a nonproductive cough and dyspnea at rest. The dyspnea worsens, and the cough becomes productive of pink, frothy sputum. Without medical intervention, lethargy, coma, and death may follow.

Symptoms of HAPE generally worsen following a night of sleep at elevation. Physical examination reveals crackles, tachycardia, tachypnea, and hypoxia. Diagnosis requires at least two of the following signs:

  • Crackles or wheezing in at least one lung field
  • Central cyanosis
  • Tachypnea
  • Tachycardia.

In addition to the above signs, at least two of the following symptoms must also be present:

  • Dyspnea at rest
  • Cough
  • Weakness or decreased exercise performance
  • Chest tightness
  • Congestion.

Chest X-ray typically reveals patchy opacities at varying locations (Figure 2). There are often infiltrates in the right middle lobe. Ultrasound has been used to facilitate the diagnosis of HAPE in the field.13 The “comet-tail” sign is a term used to describe echogenic patterns in the lung as a result of increased lymphatic flow (Figure 3). This sign, if seen in the clinical setting of HAPE, may aid in the diagnosis and monitoring of treatment efficacy.13

Mechanism of HAPE
The mechanism of HAPE is better understood than that of AMS and HACE. In HAPE, high microvascular pressures in the lungs lead to elevated pulmonary vascular resistance and pulmonary artery pressure. Pulmonary edema ensues, but left ventricular function is preserved. Patients with a naturally low HVR, high pulmonary artery pressures at rest, preexisting pulmonary hypertension, or a previous history of HAPE are predisposed to developing the condition. Risk factors include heavy exertion, rapid ascent, cold, salt ingestion, and sleeping medications.

© Shutterstock/Telegin Sergey
    

Treatment
Decent and warming of the patient as soon as possible, along with treatment outlined below, are essential.
     Oxygen. Treatment of HAPE begins with supplemental oxygen to immediately lower pulmonary artery pressure. Oxygen should initially be administered at 4 to 6 L/min; if the patient improves clinically and can maintain oxygen saturations greater than 90%, oxygen may be decreased with a goal to maintain saturation above 90%.
     Nifedipine. Following oxygen, descent, and warming, nifedipine can be used as an adjunctive therapy. The treatment dose for HAPE is 20 to 30 mg of the sustained release form every 12 hours.3
     Salmeterol/Albuterol and Expiratory Positive Airway Pressure. The oral inhalers salmeterol or albuterol may be used for bronchodilation; however, there is little evidence to support their effectiveness in HAPE. Ventilation with expiratory positive airway pressure can be employed if available.

Prevention
For patients with a predisposition to HAPE, preventive measures should be considered prior to ascent. As with all forms of altitude illness, gradual ascent is the most effective prevention method available.
     Phosphodiesterase Inhibitors. Phosphodiesterase inhibitors act via pulmonary vasodilation to prevent HAPE in some patients. Tadalafil at a dose of 10 mg twice daily or 20 mg once daily has been shown to reduce the incidence of HAPE.14 Alternatively, sildenafil 50 mg three times daily may be used.
     Acetazolamide and β-Agonists. Although both acetazolamide and β-agonists such as albuterol have been theorized to aid in preventing HAPE, this has not been proven.15

 

 

Conclusion

Clinically, high-altitude illnesses range from subtle symptoms to severe, life threatening disease. Knowledge of these disease processes and clinical presentation prior to travel or work in a high-altitude setting is essential. Rapid recognition of symptoms and prompt, appropriate interventions, such as descent when necessary, can significantly improve the outcomes of these conditions.

Dr Haroutunian is an emergency physician, department of emergency medicine, Exempla St Joseph Hospital, Denver, Colorado. Dr Bono is professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk.

References

  1. Hackett PH, Oelz O. The Lake Louise consensus on the definition and qualification of altitude illness. In: Sutton JR, Coates G, Houston CS, eds. Hypoxia and Mountain Medicine. Burlington, VT: Queen City Printers; 1992:327-330.
  2. Roach RC, Bärtch P, Hackett PH, Oelz O, and the Lake Louise AMS Scoring Consensus Committee. The Lake Louise Acute Mountain Sickness Scoring System. In: Hypoxia and Molecular Medicine. Proceedings of the 8th International Hypoxia Symposium. Burlington, VT: Queen City Printers; 1993:272-274.
  3. Eide RP 3rd, Asplund CA. Altitude illness: update on prevention and treatment. Curr Sports Med Rep. 2012;11(3):124-130.
  4. Milzman DP, Damergis JA, Napoli AM. Rapid ascent changes in vitals at altitude. Ann Emerg Med. 2008;51(4):536.
  5. Bärtsch P, Swenson ER. Clinical practice: Acute high-altitude illnesses. N Engl J Med. 2013;368(24):2294-2302.
  6. Hackett PH, Roach RC. Medical therapy of mountain illness. Ann Emerg Med. 1987;16(9):980-986.
  7. Lipman GS, Kanaan NC, Holck PS, Constance BB, Gertsch JH; PAINS Group. Ibuprofen prevents altitude illness: a randomized controlled trial for prevention of altitude illness with nonsteroidal anti-inflammatories. Ann Emerg Med. 2012;59(6): 484-490.
  8. Seupaul RA, Welch JL, Malka ST, Emmett TW. Pharmacologic prophylaxis for acute mountain sickness: a systematic shortcut review. Ann Emerg Med. 2012; 59(4):307-317.
  9. Jafarian S, Gorouhi F, Salimi S, Lotfi J. Sumatriptan for prevention of acute mountain sickness: randomized clinical trial. Ann Neurol. 2007;62(3):273-277.
  10. Jafarian S, Abolfazli R, Gorouhi F, Rezaie S, Lotfi J. Gabapentin for prevention of hypobaric hypoxia-induced headache: randomized double-blind clinical trial. J Neurol Neurosurg Psychiatry. 2008;79(3): 321-323.
  11. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280(22):1920-1925.
  12. Gallagher SA1, Hackett PH. High-altitude illness. Emerg Med Clin North Am. 2004;22(2):329-355.
  13. Fagenholz PJ, Gutman JA, Murray AF, Noble VE, Thomas SH, Harris NS. Chest ultrasonography for the diagnosis and monitoring of high-altitude pulmonary edema. Chest. 2007;131(4): 1013-1018.
  14. Leshem E1, Caine Y, Rosenberg E, Maaravi Y, Hermesh H, Schwartz E. Tadalafil and acetazolamide versus acetazolamide for the prevention of severe high-altitude illness. J Travel Med. 2012;19(5): 308-310.
  15. Schoene RB. Illnesses at high altitude. Chest. 2008;134(2):402-416.
References

  1. Hackett PH, Oelz O. The Lake Louise consensus on the definition and qualification of altitude illness. In: Sutton JR, Coates G, Houston CS, eds. Hypoxia and Mountain Medicine. Burlington, VT: Queen City Printers; 1992:327-330.
  2. Roach RC, Bärtch P, Hackett PH, Oelz O, and the Lake Louise AMS Scoring Consensus Committee. The Lake Louise Acute Mountain Sickness Scoring System. In: Hypoxia and Molecular Medicine. Proceedings of the 8th International Hypoxia Symposium. Burlington, VT: Queen City Printers; 1993:272-274.
  3. Eide RP 3rd, Asplund CA. Altitude illness: update on prevention and treatment. Curr Sports Med Rep. 2012;11(3):124-130.
  4. Milzman DP, Damergis JA, Napoli AM. Rapid ascent changes in vitals at altitude. Ann Emerg Med. 2008;51(4):536.
  5. Bärtsch P, Swenson ER. Clinical practice: Acute high-altitude illnesses. N Engl J Med. 2013;368(24):2294-2302.
  6. Hackett PH, Roach RC. Medical therapy of mountain illness. Ann Emerg Med. 1987;16(9):980-986.
  7. Lipman GS, Kanaan NC, Holck PS, Constance BB, Gertsch JH; PAINS Group. Ibuprofen prevents altitude illness: a randomized controlled trial for prevention of altitude illness with nonsteroidal anti-inflammatories. Ann Emerg Med. 2012;59(6): 484-490.
  8. Seupaul RA, Welch JL, Malka ST, Emmett TW. Pharmacologic prophylaxis for acute mountain sickness: a systematic shortcut review. Ann Emerg Med. 2012; 59(4):307-317.
  9. Jafarian S, Gorouhi F, Salimi S, Lotfi J. Sumatriptan for prevention of acute mountain sickness: randomized clinical trial. Ann Neurol. 2007;62(3):273-277.
  10. Jafarian S, Abolfazli R, Gorouhi F, Rezaie S, Lotfi J. Gabapentin for prevention of hypobaric hypoxia-induced headache: randomized double-blind clinical trial. J Neurol Neurosurg Psychiatry. 2008;79(3): 321-323.
  11. Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA. 1998;280(22):1920-1925.
  12. Gallagher SA1, Hackett PH. High-altitude illness. Emerg Med Clin North Am. 2004;22(2):329-355.
  13. Fagenholz PJ, Gutman JA, Murray AF, Noble VE, Thomas SH, Harris NS. Chest ultrasonography for the diagnosis and monitoring of high-altitude pulmonary edema. Chest. 2007;131(4): 1013-1018.
  14. Leshem E1, Caine Y, Rosenberg E, Maaravi Y, Hermesh H, Schwartz E. Tadalafil and acetazolamide versus acetazolamide for the prevention of severe high-altitude illness. J Travel Med. 2012;19(5): 308-310.
  15. Schoene RB. Illnesses at high altitude. Chest. 2008;134(2):402-416.
Issue
Emergency Medicine - 46(5)
Issue
Emergency Medicine - 46(5)
Page Number
202-210
Page Number
202-210
Publications
Emergency Medicine
MDedge Emergency Medicine
Publications
Emergency Medicine
MDedge Emergency Medicine
Topics
Sports Medicine
Imaging
Mental Health
Cardiology
Pulmonology
Article Type
Article
Display Headline
High-Altitude Illness
Display Headline
High-Altitude Illness
Article Source

PURLs Copyright

Inside the Article

Teaser Media

Recognizing and Managing Lead and Mercury Poisonings

Article Type
Article
Changed
Wed, 12/12/2018 - 19:56
Display Headline
Recognizing and Managing Lead and Mercury Poisonings
Author(s)
Christian Balmadrid, MD
Michael J. Bono, MD

Article PDF
041090035.pdf
Author and Disclosure Information

Christian Balmadrid, MD, and Michael J. Bono, MD

Issue
Emergency Medicine - 41(9)
Publications
Emergency Medicine
MDedge Emergency Medicine
Page Number
35-36
Legacy Keywords
heavy metals, lead, mercury, poisonings, toxicity, toxicologyheavy metals, lead, mercury, poisonings, toxicity, toxicology
Sections
Clinical Review
Case Reports
Author(s)
Christian Balmadrid, MD
Michael J. Bono, MD
Author(s)
Christian Balmadrid, MD
Michael J. Bono, MD
Author and Disclosure Information

Christian Balmadrid, MD, and Michael J. Bono, MD

Author and Disclosure Information

Christian Balmadrid, MD, and Michael J. Bono, MD

Article PDF
041090035.pdf
Article PDF
041090035.pdf

Issue
Emergency Medicine - 41(9)
Issue
Emergency Medicine - 41(9)
Page Number
35-36
Page Number
35-36
Publications
Emergency Medicine
MDedge Emergency Medicine
Publications
Emergency Medicine
MDedge Emergency Medicine
Article Type
Article
Display Headline
Recognizing and Managing Lead and Mercury Poisonings
Display Headline
Recognizing and Managing Lead and Mercury Poisonings
Legacy Keywords
heavy metals, lead, mercury, poisonings, toxicity, toxicologyheavy metals, lead, mercury, poisonings, toxicity, toxicology
Legacy Keywords
heavy metals, lead, mercury, poisonings, toxicity, toxicologyheavy metals, lead, mercury, poisonings, toxicity, toxicology
Sections
Clinical Review
Case Reports
Article Source

PURLs Copyright

Inside the Article

Article PDF Media
Subscribe to Michael J. Bono, MD